Evidence map›Paper›PMID 26511813›Full record

ArticleCancer research and treatment2016

Caveolin-1 Modulates Docetaxel-Induced Cell Death in Breast Cancer Cell Subtypes through Different Mechanisms.

Jinho Kang, Joo Hee Park, Hye Jin Lee, Ukhyun Jo, Jong Kuk Park, Jae Hong Seo, Yeul Hong Kim, Insun Kim, Kyong Hwa Park

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Cancer research and treatment, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 30 citations in OpenAlex.

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  15. Caveolin-1: An Oxidative Stress-Related Target for Cancer Prevention.Oxidative medicine and cellular longevity · 2017
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Jinho KangDivision of Oncology/Hematology, Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea.
Joo Hee ParkDivision of Oncology/Hematology, Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea.
Hye Jin LeeDivision of Oncology/Hematology, Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea.
Ukhyun JoDivision of Oncology/Hematology, Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea.
Jong Kuk ParkDivision of Radiation Cancer Biology, Korea Institute of Radiological & Medical Sciences, Seoul, Korea.
Jae Hong SeoDivision of Oncology/Hematology, Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea.
Yeul Hong KimDivision of Oncology/Hematology, Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea.
Insun KimDepartment of Pathology, Korea University College of Medicine, Seoul, Korea.
Kyong Hwa ParkDivision of Oncology/Hematology, Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea.
Korea University · KRKorea Institute of Radiological and Medical Sciences · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeCaveolin-1 (CAV-1) expression is more associated with basal-like cancers than estrogen receptor- or ErbB-2-expressing breast cancers. However, the biological relevance of different levels of CAV-1 expression according to subtype in the epithelial compartment of breast cancer remains unclear. MATERIALS AND

methodsWe investigated whether CAV-1 functions as a tumor suppressor and/or modulator of the cytotoxic activity of docetaxel (DTX) in subtypes of breast cancer using in vitro and xenograft models.

resultsThe levels of CAV-1 expression were closely associated with DTX sensitivity in triple-negative breast cancer cells. In addition, CAV-1 significantly inhibited cell proliferation and modulated DTX-induced apoptosis through cell cycle arrest in the G2/M phase. The mechanisms underlying DTX-induced apoptosis differed in breast cancers according to the levels of CAV-1 expression. DTX robustly enhanced Bcl-2 inactivation by CAV-1 in MDA-MB-231 cells, while p53-mediated cell cycle arrest by DTX was more pronounced in CAV-1-low but p53-functional MCF-7 cells. In parallel with the data from breast cancer cell lines, CAV-1-transfected MCF-7 cells showed higher efficacy of DTX treatment in a xenograft model.

conclusionWe clearly demonstrated cooperative effects between CAV-1 and DTX in mediating apoptosis, suggesting that the levels of CAV-1 expression might be an important indicator for DTX use in breast cancer.

Indexed as

AnimalsApoptosisCaveolin 1Cell Cycle CheckpointsDocetaxelFemaleHumansMCF-7 CellsMiceMice, Inbred BALB CReceptors, EstrogenTaxoidsTriple Negative Breast NeoplasmsTumor Suppressor Protein p53Xenograft Model Antitumor AssaysCaveolin 1DocetaxelReceptors, EstrogenTaxoidsTP53 protein, humanTumor Suppressor Protein p53ApoptosisBreast neoplasmCaveolin-1Docetaxel

Identifiers

PMID26511813
PMCPMC4843731
OpenAlexW2213871958

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.